Nature aging最新文献_第10页

Uncovering a gut microbiota-derived metabolite that triggers host cellular senescence 揭示引发宿主细胞衰老的肠道微生物衍生代谢物。

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Nature aging Pub Date : 2025-02-17 DOI: 10.1038/s43587-025-00831-3

引用次数: 0

Studying aging in the wild can help us to understand resilience and healthy aging 在野外研究衰老可以帮助我们理解适应力和健康衰老。

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Nature aging Pub Date : 2025-02-17 DOI: 10.1038/s43587-025-00829-x

Daniel H. Nussey

引用次数: 0

An mTOR paradox in sarcopenia via BCAA catabolism 肌少症通过BCAA分解代谢的mTOR悖论。

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Nature aging Pub Date : 2025-02-13 DOI: 10.1038/s43587-025-00815-3

Jerome N. Feige

引用次数: 0

Soluble cerebral Aβ protofibrils link Aβ plaque pathology to changes in CSF Aβ42/Aβ40 ratios, neurofilament light and tau in Alzheimer’s disease model mice 可溶性脑 Aβ 原纤维将 Aβ 斑块病理学与阿尔茨海默病模型小鼠脑脊液 Aβ42/Aβ40 比率、神经丝光和 tau 的变化联系起来。

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Nature aging Pub Date : 2025-02-12 DOI: 10.1038/s43587-025-00810-8

Emelie Andersson, Nils Lindblom, Shorena Janelidze, Gemma Salvadó, Eleni Gkanatsiou, Linda Söderberg, Christer Möller, Lars Lannfelt, Junyue Ge, Jörg Hanrieder, Kaj Blennow, Tomas Deierborg, Niklas Mattsson-Carlgren, Henrik Zetterberg, Gunnar Gouras, Oskar Hansson

{"title":"Soluble cerebral Aβ protofibrils link Aβ plaque pathology to changes in CSF Aβ42/Aβ40 ratios, neurofilament light and tau in Alzheimer’s disease model mice","authors":"Emelie Andersson, Nils Lindblom, Shorena Janelidze, Gemma Salvadó, Eleni Gkanatsiou, Linda Söderberg, Christer Möller, Lars Lannfelt, Junyue Ge, Jörg Hanrieder, Kaj Blennow, Tomas Deierborg, Niklas Mattsson-Carlgren, Henrik Zetterberg, Gunnar Gouras, Oskar Hansson","doi":"10.1038/s43587-025-00810-8","DOIUrl":"10.1038/s43587-025-00810-8","url":null,"abstract":"The Aβ42/Aβ40 ratio in the cerebrospinal fluid (CSF) and the concentrations of neurofilament light (NfL) and total tau (t-tau) are changed in the early stages of Alzheimer’s disease (AD)1, but their neurobiological correlates are not entirely understood. Here, we used 5xFAD transgenic mice to investigate the associations between these CSF biomarkers and measures of cerebral Aβ, including Aβ42/Aβ40 ratios in plaques, insoluble fibrillar deposits and soluble protofibrils. A high Aβ42/Aβ40 ratio in soluble protofibrils was the strongest independent predictor of low CSF Aβ42/Aβ40 ratios and high CSF NfL and t-tau concentrations when compared to Aβ42/Aβ40 ratios in plaques and insoluble fibrillar deposits. Furthermore, the Aβ42/Aβ40 ratio in soluble protofibrils fully mediated the associations between the corresponding ratio in plaques and all the investigated CSF biomarkers. In AppNL-G-F/NL-G-F knock-in mice, protofibrils fully mediated the association between plaques and the CSF Aβ42/Aβ40 ratio. Together, the results suggest that the Aβ42/Aβ40 ratio in CSF might better reflect brain levels of soluble Aβ protofibrils than insoluble Aβ fibrils in plaques in AD. Furthermore, elevated concentrations of NfL and t-tau in CSF might be triggered by increased brain levels of soluble Aβ protofibrils. Andersson et al. identify that high Aβ42/Aβ40 ratios in brain protofibrils best predict lower Aβ42/Aβ40 ratios in the cerebrospinal fluid (CSF) and higher neurofilament light/total tau levels, indicating that CSF changes in Alzheimer’s disease reflect soluble protofibrils more accurately than amyloid plaques.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 3","pages":"366-375"},"PeriodicalIF":17.0,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s43587-025-00810-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143412173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Oligodendrocyte ankyrin G in aging 少突胶质细胞锚定蛋白G在衰老中的作用。

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Nature aging Pub Date : 2025-02-12 DOI: 10.1038/s43587-025-00826-0

George Andrew S. Inglis

引用次数: 0

Effect of cholinergic modulator in Parkinson’s disease with cognitive impairment 胆碱能调节剂在帕金森病伴认知障碍中的作用。

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Nature aging Pub Date : 2025-02-10 DOI: 10.1038/s43587-025-00825-1

Yahyah Aman

引用次数: 0

Recommendations for implementing the Hevolution Alliance for Aging Biomarkers initiative 实施老化生物标志物进化联盟倡议的建议。

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Nature aging Pub Date : 2025-02-06 DOI: 10.1038/s43587-025-00812-6

Toshiko Tanaka, Felipe Sierra, Vadim N. Gladyshev, Tony Wyss-Coray, Ana Maria Cuervo, Viviana Perez, Luigi Ferrucci, On behalf of the Hevolution Alliance for Aging Biomarkers

引用次数: 0

Multiomics atlas reveals molecular and genetic drivers of human ovarian aging 多组学图谱揭示了人类卵巢衰老的分子和遗传驱动因素。

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Nature aging Pub Date : 2025-02-05 DOI: 10.1038/s43587-025-00821-5

引用次数: 0

Transdisciplinary links between societal inequality and brain structure and dynamics 社会不平等与大脑结构和动态之间的跨学科联系。

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Nature aging Pub Date : 2025-02-05 DOI: 10.1038/s43587-025-00822-4

引用次数: 0

Multi-omic profiling of sarcopenia identifies disrupted branched-chain amino acid catabolism as a causal mechanism and therapeutic target 肌少症的多组学分析确定了中断的支链氨基酸分解代谢是一种因果机制和治疗靶点。

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Nature aging Pub Date : 2025-02-05 DOI: 10.1038/s43587-024-00797-8

Xinrong Zuo, Rui Zhao, Minming Wu, Yanyan Wang, Shisheng Wang, Kuo Tang, Yang Wang, Jie Chen, Xiaoxiang Yan, Yang Cao, Tao Li

{"title":"Multi-omic profiling of sarcopenia identifies disrupted branched-chain amino acid catabolism as a causal mechanism and therapeutic target","authors":"Xinrong Zuo, Rui Zhao, Minming Wu, Yanyan Wang, Shisheng Wang, Kuo Tang, Yang Wang, Jie Chen, Xiaoxiang Yan, Yang Cao, Tao Li","doi":"10.1038/s43587-024-00797-8","DOIUrl":"10.1038/s43587-024-00797-8","url":null,"abstract":"Sarcopenia is a geriatric disorder characterized by a gradual loss of muscle mass and function. Despite its prevalence, the underlying mechanisms remain unclear, and there are currently no approved treatments. In this study, we conducted a comprehensive analysis of the molecular and metabolic signatures of skeletal muscle in patients with impaired muscle strength and sarcopenia using multi-omics approaches. Across discovery and replication cohorts, we found that disrupted branched-chain amino acid (BCAA) catabolism is a prominent pathway in sarcopenia, which leads to BCAA accumulation and decreased muscle health. Machine learning analysis further supported the causal role of BCAA catabolic dysfunction in sarcopenia. Using mouse models, we validated that defective BCAA catabolism impairs muscle mass and strength through dysregulated mTOR signaling, and enhancing BCAA catabolism by BT2 protects against sarcopenia in aged mice and in mice lacking Ppm1k, a positive regulator of BCAA catabolism in skeletal muscle. This study highlights improving BCAA catabolism as a potential treatment of sarcopenia. Using multi-omics analysis, Zuo, Zhao, Wu, Wang, Wang and colleagues report disrupted branched-chain amino acid (BCAA) catabolism in skeletal muscle samples from patients with sarcopenia. In mouse models, they causally link BCAA catabolic dysfunction to impaired muscle mass and demonstrate the translational potential of enhancing BCAA catabolism.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 3","pages":"419-436"},"PeriodicalIF":17.0,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143257538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0